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Science 14 February 1997:
Vol. 275. no. 5302, pp. 967 - 969
DOI: 10.1126/science.275.5302.967
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Reports

Somatic Frameshift Mutations in the BAX Gene in Colon Cancers of the Microsatellite Mutator Phenotype

Nicholas Rampino, Hiroyuki Yamamoto, Yurij Ionov, Yan Li, Hisako Sawai, John C. Reed, Manuel Perucho *

Cancers of the microsatellite mutator phenotype (MMP) show exaggerated genomic instability at simple repeat sequences. More than 50 percent (21 out of 41) of human MMP+ colon adenocarcinomas examined were found to have frameshift mutations in a tract of eight deoxyguanosines [(G)8] within BAX, a gene that promotes apoptosis. These mutations were absent in MMP- tumors and were significantly less frequent in (G)8 repeats from other genes. Frameshift mutations were present in both BAX alleles in some MMP+ colon tumor cell lines and in primary tumors. These results suggest that inactivating BAX mutations are selected for during the progression of colorectal MMP+ tumors and that the wild-type BAX gene plays a suppressor role in a p53-independent pathway for colorectal carcinogenesis.

The Burnham Institute, La Jolla Cancer Research Center, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA.
*   To whom correspondence should be addressed.

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Initiation of Human Astrocytoma by Clonal Evolution of Cells with Progressive Loss of p53 Functions in a Patient with a 283H TP53 Germ-line Mutation: Evidence for a Precursor Lesion.
G. Fulci, N. Ishii, D. Maurici, K. M. Gernert, P. Hainaut, B. Kaur, and E. G. Van Meir (2002)
Cancer Res. 62, 2897-2905
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Low Mutation Incidence in Polymorphic Noncoding Short Mononucleotide Repeats in Gastrointestinal Cancer of the Microsatellite Mutator Phenotype Pathway.
K. Suzuki, T. Dai, I. Suzuki, Y. Dai, K. Yamashita, and M. Perucho (2002)
Cancer Res. 62, 1961-1965
   Abstract »    Full Text »    PDF »
Loss of Bax Alters Tumor Spectrum and Tumor Numbers in ARF-deficient Mice.
C. M. Eischen, J. E. Rehg, S. J. Korsmeyer, and J. L. Cleveland (2002)
Cancer Res. 62, 2184-2191
   Abstract »    Full Text »    PDF »
PolyA Deletions in Hereditary Nonpolyposis Colorectal Cancer : Mutations Before a Gatekeeper.
K.-M. Kim, R. Salovaara, J.-P. Mecklin, H. J. Jarvinen, L. A. Aaltonen, and D. Shibata (2002)
Am. J. Pathol. 160, 1503-1506
   Abstract »    Full Text »    PDF »
Requirement of BAX for TRAIL/Apo2L-induced Apoptosis of Colorectal Cancers: Synergism with Sulindac-mediated Inhibition of Bcl-xL.
R. Ravi and A. Bedi (2002)
Cancer Res. 62, 1583-1587
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Target Gene Mutation Profile Differs between Gastrointestinal and Endometrial Tumors with Mismatch Repair Deficiency.
A. Duval, M. Reperant, A. Compoint, R. Seruca, G. N. Ranzani, B. Iacopetta, and R. Hamelin (2002)
Cancer Res. 62, 1609-1612
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Immunohistochemistry Versus Microsatellite Instability Testing in Phenotyping Colorectal Tumors.
N. M. Lindor, L. J. Burgart, O. Leontovich, R. M. Goldberg, J. M. Cunningham, D. J. Sargent, C. Walsh-Vockley, G. M. Petersen, M. D. Walsh, B. A. Leggett, et al. (2002)
J. Clin. Oncol. 20, 1043-1048
   Abstract »    Full Text »    PDF »
BAX and p16INK4A are independent positive prognostic markers for advanced tumour stage of nonsmall cell lung cancer.
C. Gessner, U. Liebers, H. Kuhn, P. Stiehl, C. Witt, J. Schauer, and G. Wolff (2002)
Eur. Respir. J. 19, 134-140
   Abstract »    Full Text »    PDF »
TRAIL-induced apoptosis requires Bax-dependent mitochondrial release of Smac/DIABLO.
Y. Deng, Y. Lin, and X. Wu (2002)
Genes & Dev. 16, 33-45
   Abstract »    Full Text »    PDF »
Functional significance of concomitant inactivation of hMLH1 and hMSH6 in tumor cells of the microsatellite mutator phenotype.
S. Baranovskaya, J. L. Soto, M. Perucho, and S. R. Malkhosyan (2001)
PNAS
   Abstract »    Full Text »    PDF »
Expression of hMLH1 and hMSH2 and assessment of microsatellite instability in testicular and mediastinal germ cell tumours.
M. Devouassoux-Shisheboran, C. Mauduit, R. Bouvier, F. Berger, M. Bouras, J. P. Droz, and M. Benahmed (2001)
Mol. Hum. Reprod. 7, 1099-1105
   Abstract »    Full Text »    PDF »
Bax Loss Impairs Myc-Induced Apoptosis and Circumvents the Selection of p53 Mutations during Myc-Mediated Lymphomagenesis.
C. M. Eischen, M. F. Roussel, S. J. Korsmeyer, and J. L. Cleveland (2001)
Mol. Cell. Biol. 21, 7653-7662
   Abstract »    Full Text »    PDF »
A functional assay for mutations in tumor suppressor genes caused by mismatch repair deficiency.
H. P. Ji and M.-C. King (2001)
Hum. Mol. Genet. 10, 2737-2743
   Abstract »    Full Text »    PDF »
O6-Methylguanine-DNA Methyltransferase Promoter Hypermethylation Shifts the p53 Mutational Spectrum in Non-Small Cell Lung Cancer.
P. Wolf, Y. C. Hu, K. Doffek, D. Sidransky, and S. A. Ahrendt (2001)
Cancer Res. 61, 8113-8117
   Abstract »    Full Text »    PDF »
Microsatellite Instability in Thyroid Cancer: Hot Spots, Clinicopathological Implications, and Prognostic Significance.
M. Onda, I. Nakamura, S. Suzuki, S. Takenoshita, C.-H. Brogren, S. Stampanoni, D. Li, and N. Rampino (2001)
Clin. Cancer Res. 7, 3444-3449
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Frameshift-mutation-derived peptides as tumor-specific antigens in inherited and spontaneous colorectal cancer.
I. Saterdal, J. Bjorheim, K. Lislerud, M. K. Gjertsen, I. K. Bukholm, O. C. Olsen, J. M. Nesland, J. A. Eriksen, M. Moller, A. Lindblom, et al. (2001)
PNAS
   Abstract »    Full Text »    PDF »
A combinatorial approach for selectively inducing programmed cell death in human pancreatic cancer cells.
Z.-z. Su, I. V. Lebedeva, R. V. Gopalkrishnan, N. I. Goldstein, C. A. Stein, J. C. Reed, P. Dent, and P. B. Fisher (2001)
PNAS 98, 10332-10337
   Abstract »    Full Text »    PDF »
Apoptosis Triggered by Myc-Induced Suppression of Bcl-XL or Bcl-2 Is Bypassed during Lymphomagenesis.
C. M. Eischen, D. Woo, M. F. Roussel, and J. L. Cleveland (2001)
Mol. Cell. Biol. 21, 5063-5070
   Abstract »    Full Text »    PDF »
Instabilotyping: Comprehensive Identification of Frameshift Mutations Caused by Coding Region Microsatellite Instability.
Y. Mori, J. Yin, A. Rashid, B. A. Leggett, J. Young, L. Simms, P. M. Kuehl, P. Langenberg, S. J. Meltzer, and O. C. Stine (2001)
Cancer Res. 61, 6046-6049
   Abstract »    Full Text »    PDF »


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